FABP4 as a therapeutic host target controlling SARS-CoV-2 infection.

Host metabolic fitness is a critical determinant of infectious disease outcomes. Obesity, aging, and other related metabolic disorders are recognized as high-risk disease modifiers for respiratory infections, including coronavirus infections, though the underlying mechanisms remain unknown. Our study highlights fatty acid-binding protein 4 (FABP4), a key regulator of metabolic dysfunction and inflammation, as a modulator of SARS-CoV-2 pathogenesis, correlating strongly with disease severity in COVID-19 patients.

Enterovirus-Cardiomyocyte Interactions: Impact of Terminally Deleted Genomic RNAs on Viral and Host Functions.

Group B enteroviruses, including coxsackievirus B3 (CVB3), can persistently infect cardiac tissue and cause dilated cardiomyopathy. Persistence is linked to 5' terminal deletions of viral genomic RNAs that have been detected together with minor populations of full-length genomes in human infections. In this study, we explored the functions and interactions of the different viral RNA forms found in persistently infected patients and their putative role(s) in pathogenesis.

Efficacy of hydrophilic resin-based sealant: A systematic review and meta-analysis.

Objectives: This meta-analysis review aims to answer two questions: 1) What is the effectiveness of hydrophilic resin-based sealant (RBS) in preventing/arresting pits and fissures caries in permanent teeth, and 2) What is the retention rate of a hydrophilic RBS as compared to alternative treatments.

Data: Randomized control trials investigating the efficacy of hydrophilic RBS compared to any other (placebo) treatment for permanent teeth. Outcomes were retention rate and caries prevention/arresting.

Biallelic variants in the transcription factor PAX7 are a new genetic cause of myopathy.

Purpose: Skeletal muscle growth and regeneration rely on muscle stem cells, called satellite cells. Specific transcription factors, particularly PAX7, are key regulators of the function of these cells. Knockout of this factor in mice leads to poor postnatal survival; however, the consequences of a lack of PAX7 in humans have not been established.